The following research seeks to characterize oxygen-induced retinopathy (OIR) in the rat as an animal model for retinopathy of prematurity (ROP). The ultimate goal of the study is to elucidate the mechanism by which hyperoxia causes retinal vascular degeneration. Recently, with the increasing sophistication of premature infant care, the survival of preterm infants has increased and with it the incidence of ROP. Yet, virtually nothing is known about the specific pathophysiology of this blinding disease. It has become increasingly desirable to develop an animal model which parallels the human in both retinal ontogeny and oxygen-induced retinal pathogenicity. It is of primary importance that this model constitute a reliable protocol for oxygen-induced retinopathy in which alterations in structure and function are readily measurable and in which results are predictable. To this end, four research projects are presented using the newborn ratling: 1) a careful and quantitative survey of the effects of hyperoxic conditions on the vasculature of newborn rat retinas, employing ink-perfused retinal whole mounts, fluorescein labeling, and electron microscopy; 2) a determination of any functional deficit which may occur immediately following oxygen exposure and with time post-exposure, coupled with an attempt to correlate such deficits with morphological and biochemical alterations; 3) a determination of the susceptibility of normoxic and hyperoxic ratlings to retinal lipid peroxidation - a process which has been suggested by several researchers to be causal in certain types of retinal degenerations and which may be enhanced by high atmospheric oxygen; and 4) an attempt to augment the antioxidant properties of the ratling retina by supplementation or dietary manipulation. The ability to conduct morphometrical, electrophysiological, and biochemical determinations all on the retinas of a single animal makes this a unique and powerful approach for the study of OIR.